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CV <3 > Lecture 5: Valvular Disorders Part 1 > Flashcards

Lecture 5: Valvular Disorders Part 1 Flashcards

1
Q

What is the difference between stenosis and regurgitation?

A
  • Stenosis: Doesn’t OPEN properly.
  • Regurgitation: Doesn’t CLOSE properly.

Stenosis: harsh, clicky sound
Regurgitation: blowing, whoosh sound

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2
Q

What are the 6 clinical classifications for valvular heart disease?

A
  • Stage A: at risk
  • Stage B: mild/mod disease, asymptomatic
  • Stage C: severe disease but asymptomatic.
  • Stage C1: severe, asymptomatic, normal LV function.
  • Stage C2: severe, asymptomatic, ABnormal LV function.
  • Stage D: symptomatic
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3
Q

What are the risk factors for valvular heart disease?

A
  • Congenital defects (AS, PS, bicuspid aortic valve)
  • Aging
  • Infective endocarditis
  • Rheumatic fever
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4
Q

What are the two settings AS typically occurs in?

A
  • Congenital: leaflet abnormality (MC: bi), presenting prior to 50yo.
  • Acquired: rheumatic fever, valve calcification, degenerative stenosis, presenting after 50yo.
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5
Q

What occurs physiologically in AS and what secondary condition does it typically lead to?

A
  • Thickening and calcification of the valve leaflets.
  • Narrowed valve opening
  • Often can lead to LVH, leading to diastolic dysfunction and then systolic dysfunction.

AS opens during systole, which is during left ventricular contraction. The LV attempts to squeeze harder to push the blood through a smaller opening.

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6
Q

How does degenerative or calcified AS result from aortic sclerosis?

A

Aortic sclerosis is calcium deposition on valve leaflets, which will lead to AS.

Most common surgical valve lesion in developed countries.

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7
Q

What are the 3 risk factors for calcified AS?

A
  • HTN
  • HLD
  • Smoking
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8
Q

AS congenital abnormality image

A
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9
Q

What are the 3 cardinal symptoms of AS?

A
  • Angina: coronary hypoperfusion (usually exertional)
  • Syncope: Increased LV pressure => baroreceptors inducing peripheral vasodilation.
  • CHF

|Cardinal AS = CAS

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10
Q

Describe AS on PE.

A
  • Mid-systolic, crescendo-decrescendo
  • R 2nd ICS with radiation to carotids
  • Medium pitch, harsh quality, often loud with a thrill.
  • Best heard sitting and learning forward.

Additional potential findings:
S4 gallop
LVH on EKG
Laterally displaced, sustained apical impulse (if LVH is present)

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11
Q

What is the diagnostic modality of choice for AS and what should we see?

A
  • Echocardiography
  • Valve < 1cm2 is severe, esp if mean gradient is > 50mm Hg

AKA smaller valve.

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12
Q

What secondary diagnostic study can confirm the presence of severe AS and any CAD?

A

Cardiac catheterization

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13
Q

What is the treatment for severe AS with symptoms?

A

AVR (aortic valve replacement), either through TAVR or open.

Need anticoag as well!!!!

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14
Q

What is the anticoagulation for mechanical valve vs TAVR?

A
  • Mechanical: warfarin +/- asa
  • TAVR: 6 months of plavix + lifelong asa
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15
Q

When is balloon valvuloplasty used?

A
  • Congenital AS primarily!
  • No medical therapy has been proven to slow progression
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16
Q

What causes aortic regurgitation?

A
  • Aortic leaflets abnormality: rheumatic fever, congenital abnormalities, infective endocarditis, HTN
  • Aortic root abnormality: aortic dissection or dilation, Marfan’s
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17
Q

What does chronic AR generally lead to?

A

LVH and dilation, which eventually leads to HF.

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18
Q

How does AR typically present?

A
  • Asymptomatic for years
  • CHF symptoms
  • Exertional dyspnea
  • Fatigue
  • Angina (similar mechanism to AS)
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19
Q

Describe the PE findings of an AR murmur.

A
  • Early diastolic, decrescendo, blowing
  • High pitched, best heard in 2nd to 4th L ICS, with radiation to apex.
  • Best heard sitting and leaning forward

Additional findings:
Widened pulse pressure
S3 or S4 gallops
Low-pitched diastolic mitral murmur at apex (austin flint murmur)

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20
Q

What is the treatment for symptomatic AR?

A
  • AVR surgery
  • Vasodilator therapy (does not slow progression)
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21
Q

What is the primary difference between AR and acute AR?

A

Body is unable to compensate for the AR, so it is an emergent situation.

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22
Q

What is the life-threatening condition that results from acute AR?

A

Hemodynamic instability as the LV is unable to compensate for the increasing volume.

Eventually leads to pulmonary edema.

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23
Q

How does acute AR present?

A
  • Cardiogenic shock
  • Pale, cool extremities
  • Weak, rapid pulse

Murmur will still be present usually, but pitch will be low.

Peripheral pulses will either be weak or absent.

24
Q

What is the main diagnostic tool for acute AR? What would be expected on diagnostic tests?

A
  • STAT echocardiogram is main diagnostic tool!
  • EKG showing mod/sev LVH
  • CXR showing cardiomegaly with LV prominence
25
Q

What are the treatment options for acute AR?

A
  • Vasodilator therapy
  • Diuretics
  • Might need to add inotropes and vasopressors later.
  • Treatment of choice is still urgent AVR.
26
Q

What is the physiology of mitral stenosis?

A

Thickening and immobility of the mitral leaflets impedes flow from left atrium to left ventricle.

27
Q

What is the most common cause of mitral stenosis and what demographic is most common?

A
  • Rheumatic fever.
  • 2/3 of cases are generally women
28
Q

What is the first pathophysiologic change that tends to occur with mitral stenosis?

A

LA enlargement.

29
Q

What is the most common cause of right-sided heart failure?

A

Left-sided heart failure

Backup from the left results in increased pulmonary pressures, which eventually affects the RV.

30
Q

What happens to the LV as mitral stenosis becomes more severe?

A

Reduced SV and CO

31
Q

When do people with rheumatic MS tend to develop symptoms?

A

4th or 5th decade of life (usually 20-40 yrs post illness)

32
Q

What are the symptoms of mitral stenosis usually due to?

A
  • Pulmonary vascular congestion
  • RV failure
  • Afib
33
Q

What are the most common symptoms of mitral stenosis?

A
  • Fatigue
  • Exertional dyspnea
  • Orthopnea
  • Afib
34
Q

What is Ortner syndrome?

A

Compression of the left recurrent laryngeal nerve from a severely dilated LA resulting in hoarseness

35
Q

Describe the PE findings of mitral stenosis.

A
  • Low-pitched, rumbling, diastolic murmur
  • Best hard at apex in left lateral decubitus
  • S1 goes from loud to softer as MS progresses
  • Opening snap following S2 is typically present

Use bell for low-pitched.

If pulmonary artery pressure increases enough, P2 can be palpable.
P2 = closure of pulmonic valve
A2 = closure of aortic valve
S2 = closure of both

36
Q

What EKG findings are typical of mitral stenosis?

A
  • LA abnormality
  • AFib
  • RVH possible
37
Q

What is the characteristic rheumatic deformity seen on echo for mitral stenosis?

A

Hockey stick deformity of the anterior MV leaflet.

2/2 to fusion of commisures and tethering of tips.
Maple syrup = hockey stick

38
Q

What are the treatment options for mitral stenosis?

A
  • Beta blockers (HR control)
  • Diuretics (pulmonary relief)
  • Severe = refer!
39
Q

What are the indications for percutaneous balloon valvuloplasty?

A
  • Pliable, noncalcified leaflets and chords
  • Minimal MR
  • No evidence of LA thrombus

Not definitive for mitral stenosis

40
Q

What are the primary causes of MR?

A
  • MV prolapse
  • LV dilation (Cardiomyopathy)
  • Posterior wall MI
  • Rheumatic fever
  • Endocarditis

Regurgitant blood flow from LV to LA during SYSTOLE.

AKA the mitral valve didn’t close properly, so instead of blood only going to the aorta, its leaking backwards to the LA.

41
Q

How do most patients with chronic MR typically present?

A

Asymptomatic and well-compensated until LV systolic dysfunction occurs.

42
Q

What are the usual symptoms of depressed LV systolic function?

A
  • Fatigue
  • Dyspnea on exertion
  • Peripheral edema
43
Q

Describe the PE findings of a MR murmur.

A
  • Holosystolic murmur
  • Best heard at apex, with radiation to axilla and back.
  • If MVP is present, mid-systolic click may be present.
44
Q

What EKG changes may occur due to MR?

A
  • LA abnormality, LVH
  • AFib
45
Q

When is coronary angiography indicated for MR?

A
  • Male > 40
  • Menopausal woman with RF
46
Q

What is the medical treatment for MR?

A
  • Afterload reduction via vasodilators (ACE/hydralazine)
  • Diuretics for pulmonary symptoms
47
Q

What is the definitive treatment for MR and when must it occur?

A
  • Surgical intervention
  • Must occur prior to irreversible myocyte damage and LV remodeling.
  • Need annual echos!
48
Q

What are the two surgical treatments for MR?

A
  • Mitral annuloplasty (sewing in a prothestic ring)
  • Mitral valve replacement (if overly calcified)
49
Q

Why is acute MR an emergent situation?

A

Cardiogenic shock due to increased LA pressure without LA dilation.

Pulmonary pressure then increases drastically.

50
Q

What are the primary causes of acute MR?

A
  • Acute MI (usually posterior wall)
  • Trauma
  • Endocarditis
  • Tachyarrhythmia with chronic MR
  • MVP
51
Q

How does a patient with acute MR present?

A
  • Signs of cardiogenic shock
  • Low-pitched, soft murmur in early systole
  • Need urgent valve replacement
52
Q

Who is MVP MC in?

A

Women

Usually younger and thinner with chest wall deformity.

Can be inherited as autosomal dominant.

53
Q

What is MVP?

A

Superior displacement in ventricular systole of one or both MV leaflets across the plane of the mitral annulus towards the LA

Outpouching that does not immediately cause MR.

54
Q

What are the symptoms of MVP syndrome?

A
  • Chest pain
  • Palpitations
  • Dizziness
  • Anxiety
  • Fatigue
55
Q

Describe the PE findings of MVP.

A

Mid-systolic click, with late systolic murmur

56
Q

Why does standing have an earlier MVP click?

A

Heart compensates by pumping with more force.

57
Q

What is the treatment for mild MVP without MR?

A

No intervention.

Need to monitor for progression to MR.

CV <3 (25 decks)

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